Electronic apparatus and method for treating human pain through application of an electrical stimulus in combination with application of a magnetic field

ABSTRACT

A medical electronic apparatus for treating human pain by the application of an electrical stimulus with the proper current density and a special magnetic flux generator stimulus to the body surface of animals which includes an electrode complex of the treatment device which includes an adhesive means for holding the 4 electrodes of the device in contact with the human body. The electrode complex is preferably comprised of 4 electrodes which are 2 positive and 2 negative electrode defining opposite diagonal vertices of the quadrilateral shape. The electrodes are supplied by power means to activate and generate an electrical stimulus. Each electrode pad contains a Magna Bloc™ which snaps into position by an aluminum snap.

This application is a continuation of U.S. patent application Ser. No.08/665,831, entitled “A Continuous Pulse, Non-Modulated Non-Burst ModeNerve Stimulator and Method of Applying Same”, filed Jun. 19, 1996,which has issued as U.S. Pat. No. 5,941,902, filed Aug. 24, 1999,incorporated herein by reference. This application further incorporatesby reference, and claims the priority of, U.S. Provisional PatentApplication Ser. No. 60/000,317, entitled “Treatment Device for Seizuresand Cerebral Edema”, filed Jun. 19, 1995; U.S. Provisional PatentApplication Ser. No. 60/000,300, entitled “Treatment Device for CardiacDysrhythmia”, filed Jun. 19, 1995; U.S. Provisional Patent ApplicationSer. No. 60/000,299; entitled “Treatment Device for Acute Burns”, filedJun. 19, 1995; U.S. Provisional Patent Application Ser. No. 60/000,318,entitled “Method of Improving Efficacy and Sensory Tolerance With aContinuous Pulse, Non-Modulating Non-Burst Mode Nerve Stimulator”, filedJun. 19, 1995; and U.S. Provisional Patent Application Ser. No.60/001,012, entitled “Method of Inducing Regional Analgesia and/orAnesthesia With a Quadrapolar Static Magnetic Field Augmented by aContinuous Pulse, Non-Modulated Non-Burst Mode Nerve Stimulator”, filedJul. 10, 1995.

BACKGROUND OF THE INVENTION

Field of the Invention

This invention relates to the field of medical electronics and moreparticularly to apparatus for treating human pain by application of anelectrical stimulus with the proper current density to the body surfaceand the response modulated by a magnetic field to allow manipulation ofthe firing rate of peripheral neurons of the A-fiber and C-fibernociceptors such that chronic and acute pain may be consistentlycontrolled without discomfort from the stimulation.

SUMMARY OF THE INVENTION

Maurer, et., al., 1994 (U.S. Pat. No. 4,431,002) indicates that it iswell known that pain can be alleviated by electrical pulses applied tothe surface of the body or to electrodes implanted within the body. Hisinvention revealed a transcutaneous electrical nerve stimulationapparatus in which the stimulus pulses are modulated in both time andintensity in a prescribed manner, the pulse amplitude and widthdecreasing, while the pulse repetition rate increases and vice versa.The advantage of this arrangement is said to produce a comfortable andpleasant sensation at levels sufficient to produce muscle contractionand stimulation of deep afferent nerves to cause the release ofendogenous opiates, such as endorphins, which are thought to suppresspain.

Deyo, et., al., (NEJM) concluded that Transcutaneous Electrical NerveStimulation (TENS) in patients with chronic low back pain is no moreeffective than treatment with placebo, and TENS adds no apparent benefitto that of exercise alone. It is apparent that such studies are donewithout the proper application and use of the technology. It is furtherapparent that technology is needed that is easier to understand and useby the operator.

The reduction of efficacy of a C-fiber input by coactivation ofmechanoceptive A-fibers is the principle underlying transcutaneouselectrical nerve stimulation (TENS). The mechanism involved is referredto as the “Gate Control Theory of Pain Perception” (See FIG. 5). TENSinvolves electrical activation of mechanoceptive fibers. MechanoceptiveA-fibers are activated at lower electrical stimulation intensities thanC-fibers, that is, A-fibers have a low threshold. Thus, themechanoceptive A-fibers can be selectively activated by low intensityelectrical stimulation without increasing the firing rate of C-fibers,that is, A-fibers can be selectively activated by low intensityelectrical stimulation without increasing the firing rate of C-fibers.As the intensity of stimulation is increased, it is possible to activateboth mechanoceptive and nociceptive fibers. Thus, there is a limit tohow much stimulation can be applied in order for the current TENS towork. Patients who use TENS devices are fully aware that if theycontinue to increase the stimulus intensity, they have more pain, ratherthan less pain. The increasing pain with stimulation is because ofC-fiber activation. In some cases, the intensity of stimulation requiredto achieve pain relief can be reduced simply by repositioning electrodesand reducing the current flux through tissues while still reachingA-fiber threshold. In other cases, it is not possible to achieve painrelief at sufficiently low intensities to selectively activate A-fibers.In these cases, pain may be increased and TENS is said to have failed.In these cases of failure, the information available suggests that TENSfailure is largely due to inappropriate electrode placement andinsufficient current flow or density at the point of desiredstimulation.

Evidence from the literature, clinical observations and isolatedneuronal cell preparation data suggest that efficacy of this device isbest obtained by high frequency, continuous stimulation with highcurrent density in the area of stimulation. Pacing of A-fibers alongwith simultaneous suppression of C-fiber firing provides reliablecontrol of pain syndromes. For the efficacy of the invention to berealized, a quadripolar array of positive and negative electrodes arearranged in quadrilateral array such that the positive and negativeelectrodes are in the proper close proximity to one another such thathigh current density can be obtained in the area of the nerve fiber tobe paced. It is a further object of this invention to suppress thefiring rates of C-fibers while increasing the rate of A-fibers. Thisobject is accomplished by placing a Magna Bloc™ device within thestimulating electrode. This device, as will be demonstrated later,dramatically controls and reduces C-fiber firing. This effect on C-fiberfiring is dramatically illustrated in FIG. 6. Volunteer subjectsperceived the pain threshold at two (2) times the voltage (whichtranslates to current flow) when the Magna Bloc™ device was placed overthe stimulating electrodes. Through this methodology, normal firingpatterns can be sent to the central nervous system, frequency coded, fora sensation of comfort rather than pain.

The device of this invention consists of 4 electrodes per unit. Theelectrodes consist of 4 electrodes of alternating polarity and consistof 2 positive poles and 2 negative poles. The positive and negativepoles of the electrode head are aligned in substantially a single planeand are oriented in a quadrilateral configuration with positive polesoriented diagonally opposite one another and negative poles orienteddiagonally opposite one another. Built into each electrode is a MagnaBloc™ device U.S. Pat. No. 5,312,321 (incorporated herein by reference).This device allows maximal A-fiber stimulation without the discomfort ofC-fiber pain and muscle contraction. The Magna Bloc™ controls theexcitability of neuromuscular units and blocks C-fiber firing.

Another object of the invention is to maintain current densitysufficient to send A-fiber impulses into the dorsal horn in the area ofthe innervation of the C-fibers involved in the pain syndrome, insufficient density to block C-fiber input into the central nervoussystem. This is accomplished by placing electrodes in the correctproximity to each other using the Magna Bloc™ to control C-fiber firingwhen the intensity is turned up to above usual C-fiber threshold and byplacing a current sensor in the midpoint between the 4 electrodes. Thissensor will balance the current density by rotating monitoring of the 4electrodes and compensating by changing the input such that currentdensity or current flow in the skin remains constant. This circuit willhave a range monitor and alarm system. Current flow will alternate every2 seconds in electrodes in FIG. 1 B to A and C to D, C to A and B to D.

It is a further purpose of this invention to have two or more such 4electrode arrays per TENS unit.

Except as noted above, the unit uses standard TENS electronics with thefollowing parameters:

1) the parameters are intensity of output is 0 to 100 mA, frequency 0 to200 Hzt, pulse width 400 microseconds. The device is effective eitherover the dorsal columns or on afferent nerve bundle as well as over thearea of pain sensation. The containment means to hold the 4 electrodes,4 Magna Bloc™ devices and current density sensor and electrode padsprovides a method of therapeutically placing an alternating electrode DCfrequency modulated device on the human body to relieve pain, which haswell controlled current density in which C-fiber firing is controlled bya Magna Bloc™ field which generates a flux field gradient in the “2”axis of 60° to 70°.

This aspect may further provide repetition of these steps for additionalcontainment bodies for attachment to the human body at additionalplacement positions.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a prospective view of the treatment device electrodesaccording to one embodiment of the invention.

FIG. 2 is a plan view of the treatment device which powers the electrodeof FIG. 1.

FIG. 3 is a block diagram of electrical stimulation apparatus accordingto the invention (FIG. to follow).

FIG. 3 depicts useful locations for the placement of the electrodes ofthe invention.

FIG. 4 depicts in graphic form field intensity of the magneticquadripolar portion of the electrodes of the device, as determined byscanning in a systematic parallel plane 0.3 cm above the surface of theMagna Bloc™ device.

FIG. 5 is the Gate Theory of Pain Perception and

FIG. 6 is the change in somatosensory thresholds to electrical stimuluswhen treated with Magna Bloc™.

FIG. 7 illustrates the schematic representation of anatomicalconnections associated with pain perception and

FIGS. 8-14 illustrate graphical representations of treatment for pain onsubjects.

DESCRIPTION OF THE PREFERRED EMBODIMENT

Reference will now be made in detail to the presently preferredembodiments of the invention, examples of which are illustrated in theaccompanying drawings. Throughout the drawings, like referencecharacters are used to designate like elements.

The electrode complex of the treatment device of the current inventionis schematically illustrated in FIG. 1. Treatment device electrode 10includes an adhesive means 11 for holding the electrodes 12 and theMagna Bloc™ Devices 13 in contact with the human body. According to theinvention, electrode 12 is preferably comprised of 4 electrodes, 2 ofwhich are positive, 2 of which are negative and all of which areelectrodes defining opposite diagonal vertices of the quadrilateralshape. Each electrode pad contains a Magna Bloc™ which snaps in positionby an aluminum snap.

As embodied herein, Magna Bloc™ 13 (magnetic flux generator) comprisesfour substantially identical magnetic poles held in a plasticcontainment means that will hold the magnetic bodies in the desiredconfiguration (see U.S. Pat. No. 5,312,321) and which produces a 60° to70° gradient in the “z” axis (see FIG. 4). The gradient is the slope ofthe field intensity change over distance.

The embodiment of this invention further contains conducting wires 15and 16 which connect to electrode wires 21 through connectors 20. Theconducting wires 15 and 16 are contained in conducting cable 14. Furtherembodied in this invention is voltage sensor 17 with electrode connectorcables 22 which are ultimately housed in conductor cable 19.

The beneficial effects of this invention, as illustrated by FIGS. 8-14,are brought about by the ability of the system to maintain a propercurrent density or flow between the electrodes on a continuous basis inthe area of the A-fibers and C-fibers involved in the pain syndromeunder treatment. The desired current density is maintained by theelectrode pads 12 which are controlled by range monitor (within thehousing) and alarm system. The intensity of the current flow will bedictated by a voltage sensor 17. The current flow will alternate every 2seconds in electrodes B to A, C to D, C to A and B to D. The density ofcurrent flow can be operated at a much higher level than in the classicTENS due to the placement of the Magna Bloc™ device 13 within theelectrode 12. The Magna Bloc™ 13 completely relieves the discomfort ofC-fiber firing when the C-fiber threshold is exceeded. The Magna Bloc™13 blocks C-fiber firing, therefore giving a favorable balance toA-fiber/C-fiber ratio and therefore makes this device very effective inrelieving pain (see position suggestions for treatment in FIG. 3). Forthe Magna Bloc™ to control C-fiber firing it must have a field gradientof >45°<90° in the “z” axis.

The controlling mechanism of this treatment device as shown in FIG. 2contains a TENS generator unit 23 which contains the battery source,pulse generator, intensity controls 25, frequency controls 26, durationcontrols 27, current density modulation polarity switching means,current density modulation cable 19 with male connector 28 and femaleconnector 29. Cable 14 male connector plugs into female connector 24.On-off and alarm light are contained within the cabinet housing.

Supporting Experimental Data

Table of Contents

I. Introduction

a. Pain

b. Pain Pathways and Pain Sensation

c. Pain Impulse Generation

II. Methods of Interruption of Pain Impulses

a. Electrical Stimulation

b. Magna Bloc™ TMNS

III. Figures

IV. Appendix

Summary and Conclusions

The data in this document demonstrates that the invention unit willblock C-fiber mediated pain and hyperalgesia created by the intradermalinjection of capsaicin in human volunteers as seen in FIGS. 8-14. Thisresponse is well documented by current density (current flow or densityis calculated by the voltage from a stimulating electrode to anylocation of the treatment area, the resistance is calculated by an ohmcircuit, with voltage and resistance-current density may be easilycalculated) dose response curves as well as the demonstration that thearea of hyperalgesia increases in size after the unit is turned off forfive minutes (A-B-A observation). The FIGS. demonstrate the synergeticeffect of the invention on a common pathway i.e. nociceptor input intothe central nervous system.

I. Introduction

The data in this document demonstrates that the invention unit willblock C-fiber mediated pain and hyperalgesia created by the intradermalinjection of capsaicin in human volunteers. This response is welldocumented by current density (current flow or density is calculated bythe voltage from a stimulating electrode to any location of thetreatment area, the resistance is calculated by an ohm circuit, withvoltage and resistance-current density may be easily calculated) doseresponse curves in the Figures as well as the demonstration in theFigures that the area of hyperalgesia increases in size after the unitis turned off for five minutes (A-B-A observation). The Figuresdemonstrate the synergetic effect of the invention on a common pathwayi.e. nociceptor input into the central nervous system.

A. Pain. Pain is a multifactorial perception. The InternationalAssociation for the Study of Pain defines pain as “unpleasant andemotional experience associated with actual or potential tissue damage.”

B. Pain Pathways and Pain Sensation. The central nervous systemintegration of pain pathway stimulation takes place in the cerebralcortex. The Figures present a schematic representation of the anatomicalconnections associated with pain perception. The generation of theimpulse usually begins in the peripheral nociceptors. The primaryafferent neurons are largely A-delta and C-fibers. Pain intensity isrelated to the firing frequency of the impulses along the pathway. Thevarious structures which have connections along the pain pathway affectthe ultimate pain intensity and perception. Very complex circuits affectthe pain perception involving both excitatory and inhibitoryrelationships.

C. Pain Impulse Generation. The Pain impulse (i.e. volley of actionpotentials) may be generated in the nerve ending (i.e. the receptorfield) or anywhere along the pain pathway. Any stimulus or injury whichresults in repeated depolarization of the afferent neuron cell wall willresult in a volley of action potentials which are conducted into thecentral nervous system.

II. Methods of Interruption of the Pain Impulses

A. Electrical Stimulation. Various methods of electrical stimulationhave been used in an attempt to control acute and chronic pain. Thetheories have largely included: 1) The Gate Control Theory and 2) Therelease of endorphins which block pain transmission. The most widelyaccepted is the Gate Control Theory. The reduction of efficacy of aC-fiber input by co-activation of mechanoceptive A-fibers therebyincreasing the ratio of A-fiber/C-fiber is a principle mechanism. Thenet result is to increase the frequency of A-fiber firing to C-fiberfiring. This results in a net decrease in nociceptor impulses into thecentral nervous system. Mechanoceptive A-fibers are activated at lowerelectrical stimulation intensities than C-fibers, that is, A-fibers havea low threshold. Thus, the mechanoceptive A-fibers can be selectivelyactivated by low intensity electrical stimulation without increasing thefiring rate of C-fibers. As the intensity of stimulation is increased,it is possible to activate both mechanoceptive and nociceptive fibers.This decreases the ratio of A-fiber to C-fiber firing and, as thestimulus intensity increases, the patient experiences more pain, ratherthan less, because of C-fiber activation and the decreasingA-fiber/C-fiber firing ratio. In some cases, it is not possible toachieve pain relief at sufficiently low intensities to selectivelyactivate A-fibers. In these cases, pain may be increased with increasedstimulus intensity and the TENS is said to have failed.

We have demonstrated that the mechanism of this invention involvesblocking C-fiber nociceptor input into the central nervous system. Weused the capsaicin model and demonstrated that the experimental unitblocks C-fiber mediated hyperesthesia and hyperalgesia (See FIGS. 8through 14). FIG. 8 is a demonstration of the dose response of the areaof capsaicin induced hyperalgesia and hyperesthesia with increasingcurrent density. The area of hyperesthesia and hyperalgesia is expressedin cm² and the intensity is expressed as subthreshold, threshold andsuprathreshold (see appendix). The notation of 60 m means stimulationfor 60 minutes. FIG. 9 represents the change in surface hyperalgesia andhyperesthesia at threshold current for 15 minutes, 30 minutes, 60minutes and for 5 minutes at suprathreshold. The remainder of theFigures are self explanatory if reference is made to FIG. 8 or 9. FIG. 6represents the evaluation of hyperalgesia at 15 minutes, 30 minutes, 60minutes in both placebo and Magna Bloc™ treated arms, and the numbers 1to 5 on the right are the same subjects (1—1, 2—2, 3—3, 4—4 and 5—5),but the opposite arm, which is placebo treated. We also demonstratedthat the effect on blocking C-fiber transmission is related to currentdensity in the area of pain generation. We have made the unit moreeffective by changes in electrode design and have demonstrated that theGate Control mechanism is compatible with our findings.

Nociceptive C-fibers are ordinarily quiescent. However, atissue-damaging stimulus activates free nerve endings imbedded in thedermis. This transducing step involves the influx of calcium to producea generator potential. Once the generator potential reaches threshold,action potentials fire and are conducted centrally along C-fibers towardthe spinal cord. The net result is that stimulation of C-fibers altersthe ratio of A-fiber to C-fiber activation, which in turn increases thefiring rate of the T cell and leads to pain perception, according to theGate Control Theory of pain. The intensity of pain is proportional tothe firing rate of the T cell. The invention has been shown to decreasethe firing rate of C-fibers both in vitro and in vivo. The alteration inthe ratio of A-fiber/C-fiber firing rate results in pain relief.

B. Magna Bloc™ TMNS. Nociceptive C-fibers are ordinarily quiescent.However, a tissue-damaging stimulus activates free nerve endingsimbedded in the dermis. This transducing step involves the influx ofcalcium to produce a generator potential. Once the generator potentialreaches threshold, action potentials fire and are conducted centrallyalong C-fibers toward the spinal cord. The net result is thatstimulation of C-fibers alters the ratio of A-fiber to C-fiberactivation, which in turn increases the firing rate of the T cell andleads to pain perception, according to the Gate Control Theory of pain.The intensity of pain is proportional to the firing rate of the T cell.The Magna Bloc™ has been shown to decrease the firing rate of C-fibersboth in vitro and in vivo. The alteration in the ratio ofA-fiber/C-fiber firing rate results in pain relief in the same way inwhich the TENS brings about pain relief.

The Effects of Magna Bloc™ on C-Fibers Which Have Been Stimulated byCapsaicin in Human Volunteers

Introduction

This report summarizes my analysis of the data collected in March, 1991in a clinical study that was designed to test whether the treatmentdevice of this application has a therapeutic effect on the human armagainst which the device is applied. The tests were performed inconjunction with Jose Ochoa, M.D., Ph.D., DS.C. at Good SamaritanHospital and Medical Center in Portland, Oreg. Dr. Ochoa is the Directorof the Peripheral Nerve Disease Unit at Good Samaritan Hospital andMedical Center.

1. The clinical study was performed on five test subjects. Two of thetest subjects were tested two times. The test subjects ranged from 37 to50 years of age. Two subjects were female and three were male. Each ofthe test subjects was in good health. None of the test subjects weretaking any medications.

2. The tests were conducted by a test investigator and a testingassistant. Each test subject was tested one time using an “active”magnetic treatment device (Magna Bloc™). The “active” treatment deviceused in the tests had four ½ inch diameter magnets, each having amagnetic energy product of 27 MG-Oe, all encased in an opaque plastichousing. Each test subject was also tested with a “placebo” device. The“placebo” device looked and felt identical to the “active” device,except in the placebo device, the four magnets were placed with fournon-magnetic metal cylinders. The order of active or placebo testing wasrandomly selected by a coin toss. The test subject and test investigatordid not know when a specific test was using the active device or theplacebo device.

3. Each test subject was tested on one arm with the active magnetictreatment device and on the other arm with the placebo device. The armallocation (right arm or left arm first) was randomly determined by acoin toss.

4. The following procedure was followed for each test, whether the rightarm or left arm was tested and whether the treatment was active orplacebo.

A. An injection point was identified on the volar forearm of the testsubject 17.5 inches up the arm from the test subject's wrist. Theinjection point was marked with an ink dot. The treatment device (activeor placebo) was centered over and against the injection point of thetest subject's arm for 15 minutes. After 15 minutes, the treatmentdevice was removed from the test subject's forearm and a 1 microgramdose of capsaicin was injected into the test subject's arm (intradermal)at the injection point.¹ Capsaicin is the pungent active component inhot chili peppers. Capsaicin has been found to activate the c-nociceptornerve fibers in humans that convey painful stimuli to the centralnervous system.

¹One test subject showed no response to a 1 microgram dose of capsaicinand was accordingly injected with a 5 microgram dose of capsaicin.

B. Immediately following injection, the treatment device was placed backover the capsaicin injection point. At 15 minutes after the injection,the treatment device was removed briefly from the test subject's arm topermit measurement of the area of cutaneous hyperalgesia (skin pain dueto light stroking with a cotton swab). Following this measurement, thetreatment device was immediately placed back over the injection point.This procedure for measuring cutaneous hyperalgesia was repeated at 30minutes after injection.

C. At 60 minutes after injection, the treatment device was removed fromthe test subject's arms and the area of cutaneous hyperalgesia wasmeasured a third time. The area of hyperalgesia was measured at 15, 30and 60 minutes after capsaicin injection. The area of hyperalgesia isdetermined by lightly stroking the skin with a cotton swab in a mannerthat would not ordinarily cause painful sensations. The area around theinjection point where this light stroking caused pain to the testsubject was traces and measured in square centimeters. The hyperalgesiaarea measurements for test subjects appear in the table (area ofhyperalgesia).

5. Robert A. Parker is a biomedical statistician who has retained toanalyze the data from the clinical study described above. Mr. Parkerreceived a Bachelor of Science degree in Math from the MassachusettsInstitute of Technology in 1970; received a Master of Science degree inMedical Statistics from the London School of Hygiene and TropicalMedicine in 1976; and received a Doctor of Science degree inBiostatistics from the Harvard School of Public Health in 1983. Mr.Parker is currently an Assistant Professor at the Vanderbilt UniversitySchool of Medicine.

6. Mr. Parker found that the differences in results between active andplacebo treatment were statistically significant for the measurements ofarea of hyperalgesia at 15, 30 and 60 minutes.

The Effects of TENS (Transcutaneous Electrical Nerve Stimulator) onHyperesthesia and Hyperalgesia Mediated by C-fibers Which Have BeenStimulated by Capsaicin in Human Volunteers

This report summarizes my analysis of the data collected in June 1995 atthe Department of Neurology, Vanderbilt University Medical Center inNashville, Tenn. The human study was designed to test whether the TENSdevice and the Magna Bloc™ device suppress or interrupt nociceptors(C-fibers) firing in a human pain model in which 1 microgram ofcapsaicin is injected intradermally and the area of mechanicalhyperalgesia and hyperesthesia are evaluated with time. The purpose wasto evaluate substantial equivalent mechanism of action.

1. The clinical study was performed on three (3) test subjects usingboth arms for the study. Variables were time, current density andcombinations of TENS and Magna Bloc™. The test subjects ranged in agefrom 28 to 60 years. All test subjects were male and in good health.None of the subjects were taking any medications.

2. The tests were conducted by a test investigator and a testingassistant. We used an EPIX XL™ TENS unit with 4 electrodes forstimulation. The 4 electrodes of the TENS unit were placed over thecomers of a 5 cm square. The polarity of each electrode was opposite tothe electrode in the next comer and the same polarity as the electrodein the opposite corner. Each subject was tested one time using a TENSunit at subthreshold intensity in one arm and a TENS unit at thresholdintensity followed by suprathreshold intensity in the other arm.Subthreshold level was defined as the minimal intensity perceived by thesubject and Suprathreshold level was defined as the maximum intensitytolerated by the subject and described as discomfort, but not pain.

3. The following procedure was followed for each test.

A. An injection point was identified on the volar surface of the forearmof the test subject, 17.5 cm up the arm from the test subject's wrist.The injection point was marked with an ink dot. The treatment device wascentered over the injection point of the test subject's arm for 15minutes. After 15 minutes, a 1 microgram dose of capsaicin was injectedon to the subject's arm (intradermal) at the injection point. Capsaicinis the pungent active component in chili peppers. Capsaicin has beenfound to activate the c-nociceptor nerve fibers in humans, resulting inpain and secondary hyperalgesia through a polysynaptic, reflex thatconvey painful stimuli to the central nervous system.

B. The areas of hyperesthesia (increased sensation to light touch bysliding over the skin the wood piece of a cotton swab) and hyperalgesia(skin pain to light touch by sliding over the skin the wood piece of acotton swab) were measured at 15, 30 and 60 minutes after the injectionof capsaicin and 5 minutes after the use of suprathreshold stimulation,Magna Bloc™. The areas of hyperesthesia and hyperalgesia were markedwith ink lines and measured in square centimeter.

Capsaicin Model

Capsaicin is the “hot” or active portion of hot pepper. It has beendemonstrated by multiple investigators that capsaicin, when injectedinto the skin intradermally, activates exclusively afferent polymodal(C-fiber) nociceptors. Therefore, C-fiber impulses into the centralnervous system are perceived as pain. This C-fiber activation stimulatesa spinal cord reflex which stimulates the sympathetic C-fiber efferentsin the area of the capsaicin injection. C-fiber efferents overlysensitize the skin. The resultant effect is over sensitization of theskin which causes pain perception upon light touch. The area ofhyperesthesia and hyperalgesia are related to C-fiber afferent firingrates. Therefore by use of this model one may evaluate the effect oftreatment upon stimulation and conduction of painful impulses mediatedby polymodal nociceptors.

The unit basically allows consistent results on pain treatment becauseof the ability to produce symmetric current density which is selectivefor stimulation of A-fiber and suppression of C-fibers. This unit ismuch more effective and comfortable.

What is claimed:
 1. A medical electronic apparatus for treating human pain by the application of an electrical stimulus with the proper current density and a special magnetic flux generator stimulus to the body surface, comprising: an electrode complex of the treatment device comprising 4 electrodes and an adhesive means for holding the electrodes in contact with the human body; wherein the 4 electrodes further comprise 2 positive and 2 negative electrodes defining opposite diagonal vertices of a quadrilateral shape and forming an electrode pad; a power means for supplying power to activate the electrical stimulus to each electrode; the electrode pad further comprising at least one quadropolar magnetic flux generator having four center charged magnetic poles in alternating polarity for generating a three-dimensional flux field gradient >45 degrees <90 degrees in the “Z” axis.
 2. The therapeutic medical electronic apparatus of claim 1, wherein each electrode comprises at least one quadripolar magnetic flux generator having four center charged magnetic poles in alternating polarity for generating a three-dimensional flux field gradient >45 degrees <90 degrees in the “Z” axis for the purpose of modulating C-fiber activity.
 3. The therapeutic medical electronic apparatus of claim 2, wherein the quadripolar magnetic flux generator is composed of 4 circular, center charged, neodymium magnetic poles in alternating polarity.
 4. The therapeutic medical electronic apparatus of claim 2, wherein each magnetic flux generator of the invention comprises four substantially identical magnetic poles held in a plastic containment means that will hold the magnetic bodies in the desired configuration and which produces a 60° to 70° magnetic flux field gradient in the “Z” axis.
 5. A medical electronic apparatus for treating human pain by application of an electrical stimulus, the apparatus comprising: a) an electrode complex comprising at least one electrode in contact with the body surface of a human to be treated; b) each electrode further comprising at least one quadrapolar magnetic flux generator having four center charged magnetic poles in alternating polarity for generating a three-dimensional flux field gradient >45 degrees <90 degrees in the “Z” axis; and c) power means for supplying power to activate the electrical stimulus to each electrode for the purpose of modulating C-fiber activity.
 6. The apparatus of claim 5, comprising a plurality of electrodes in contact with the body surface of a human to be treated.
 7. The apparatus of claim 5, comprising four electrodes in contact with the body surface of a human to be treated.
 8. The apparatus of claim 6 or 7, wherein each electrode further comprises a plurality of quadripolar magnetic flux generators having four center charged magnetic poles in alternating polarity for generating a three-dimensional flux field gradient >45 degrees <90 degrees in the “Z” axis.
 9. The apparatus of claim 5, wherein the electrodes are placed at a sufficient distance apart from a person to be treated to allow for the proper current density in the field of stimulation when electrical stimulus is applied thereto.
 10. The apparatus of claim 5, wherein the electrode complex further comprises a single contiguous unit which includes an adhesive means for holding the electrodes in contact with the body surface.
 11. The apparatus of claim 5, wherein each quadripolar magnetic flux generator defines a means for suppressing C-fiber firing, thereby allowing a favorable ratio of A delta/C-fiber firing and thereby more efficiently blocking peripheral generated pain.
 12. The apparatus of claim 5, wherein each magnetic flux generator comprises four circular, center charged, neodymium magnetic poles.
 13. The apparatus of claim 5, wherein each magnetic flux generator generates a three-dimensional flux field gradient >60 degrees <70 degrees in the “Z” axis.
 14. The apparatus of claim 5, further comprising a means for alternating current flow to each electrode every 2 seconds.
 15. The apparatus of claim 5, further comprising a range monitor and alarm system, the range monitor and alarm system receiving sensory input data from a voltage sensor in contact with the body surface and controlling current density from the sensory input.
 16. The apparatus of claim 15, wherein the range monitor and alarm system maintains a proper current density on a continuous basis for the purpose of modulating A-fiber and C-fiber activity.
 17. The apparatus of claim 5, further comprising a TENS generator unit operatively connected to the electrode complex, the TENS generator unit further comprising a battery supplying power to the unit, a pulse generator creating a pulsed electrical current through the unit, means for controlling current intensity, density, frequency and duration through the electrode complex; and means for modulating current density and alternating current direction through the electrode complex.
 18. A method for treating human pain comprising the following steps: a) providing an electrode complex comprising at least one electrode, each electrode comprising a quadrapolar magnetic flux generator having four center charged magnetic poles in alternating polarity for generating a three dimensional flux field gradient >45 degrees <90 degrees in the “Z” axis; b) supplying a power means for activating and generating an electrical stimulus through each of the electrodes; and c) applying an electrical stimulus to the electrode complex and positioning the complex on the body surface of the human to be treated for the purpose of modulating C-fiber activity and blocking peripheral generated pain when the electrical stimulus is applied to the electrical complex. 